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Giuseppe Floridi Non-Surgical Treatment of Periapical Lesions Abstract
Periapical pathosis To emphasize the importance of bacteria, it has been demonstrated that exposed dental pulps of conventional and germ-free rats to their own oral flora resulted in the development of pulpal and periapical lesions in conventional rats, but failed to originate those lesions in germ-free rats. The major pathways of pulpal contamination are exposeed dentinal tubules, direct pulp exposure, lateral and apical foramen as well as bood-borne bacteria. As a result of the presence of germs in the dentin a variety of immunocompetent cells can be recruited to the dental pulp. As a result of the interaction of the microorganisms and their by-products, various nonspecific and specific mediators of inflamation are released. The pattern of osseous tissue breakdown in response to an irritant, coupled with microorganisms, such as that found in the periradicular bone in response to an infected root canal, has been thoroughly demonstrated.The inflammatory process that occurs in pulpal disease and degeneration is basically the same as elsewhere in the body’s connective tissue. Coupled with the inflammatory potential of endodontic procedures, coronal leakage of bacteria and their products from poor dental restorations, and/or toxic root canal filling matenals, the extension of these processes into the penradicular tissues. Histologically the lesion consists predominantly of granulation tissue, exhibiting significant angioblastic activity, many fibroblasts, connective tissue fibers, an inflammatory infiltrate, and often a connective tissue encapsulation The inflammatory infiltrate consists of plasma cells, lymphocytes, mononuclear phagocytes, and neutrophils. Occasionally cholesterol clefting is seen, as are foreing-body giant cells. If, in addition, adjacent strands of epithelium or rests of Malassez have been stimulated by the inflammatory response to form a stratified squamous epithelium-lined cavity filled with fluid or semi-solid materia, a cyst may be considered to the present. As long as there is passage of irritants from the root canal system, or a failure of the phagocytic macrophage system to control this irritation, the histological pattern of the periradicular lesion will be one of concomitant repair and destruction. This concept must be understood by the practitioner because it relates to the rationale for non surgical root canal treatment as opposed to surgical intervention. The mere surgical removal, via curettage, of the reactive periradicular tissues will not address the source of the patient’s problem, i.e. the removal of irritants from within the canal and the three- dimensional obturation of the properly cleaned and shaped canal system. The non-surgical treatment of the majority of root canals will result in complete repair of even the largest -periradicular lesions, provided the following factors are addressed: the elimination of coronal leakage around questionable or inferior dental restorations, the managment of concomitant periodontal disease, and the recognition and management of tooth defects, such as fractures or resorption. In the past, a controversy has existed among practitioners and authors that a periradicular granuloma could be differentiated from a cyst using specific radiographic criteria. The majority of periradicular lesions associated with teeth without root canal treatment are caused by pulpal inflammation and/or degeneration. Most of these periradicular lesions (>90%) can be classified as dental granulomas, radicular cysts, or abscesses. However, multiple investigation have shown that differential diagnostic radiographic criteria are unreliable. Although there are a number of studies that indicate a correlation between radiographic lesions that increase in size and the incidence of a periradicular cyst, other investigation have not been able to corroborate this correlation. It is sufficent to say that the development of these lesions is largely due to the passage of irritational products, including microorganisms, from the root canal space. Because it is clinically and radiographically impossible to differentiate between a cyst and a granuloma, judicious treatment planning should favour a conservative approach to treatment. Although there is some support for the fact that the prognosis for root canal treatment is potentially poorer in teeth, where there are such areas - of apical rarefaction prior to treatment, as opposed to e teeth without such areas, the dynamic nature of the periradicular tissue cannot be determined clinically. Even if epithelium is present within a granuloma, it is impossible to determine if it is inert or proliferating, with the eventual possibility of cyst formation. The fact that the incidence of periradicular cysts has been reported as high as 54% is clear evidence that cysts .heal as well as granulomas, following proper non-surgical root canal treatment. Regardless of this inference, there pervading opinion among practitioners that lesions be treated non-surgically and observed, while larger lesions should be surgically removed. In teeth with periradicular lesions, the removal of the irritants (inflamed or necrotic tissue) from the root canal system begins the process of repair and resolution. Repair of periradicular lesions is primarily characterized by inflammatory cell infiltration which is responsible for removal endogenous and exogenous irritants, followed by fibroblastic proliferation collagen deposition, bone formation and cemental apposition if root resorption was present. Integrated within these events are complex cellular and immunological phenomena designed to eradicate all debris and foreign material that is counterproductive to tissue repair. When a granuloma is present the course of healing is uneventful and generally follows the events described. Histological repair of the periradicular tissues generally occurs following resolution of the periradicular inflammatory response. Criteria for histological repair of periradicular tissues are the following:
While these events cannot be accurately determined radiographically, specific radiographic criteria have been provided in which a reasonable inference can be made that the histological processes of repair have been completed. Non-surgical treatment with calcium hydroxide temporary fillings. The prime focus for the practitioner is to completely biomechanically and chemo-mechanically debride and shape the root canal system regardless of the nature of the periradicular tissues. Obturation of the prepared root canal is essential, with a well-condensed filling material, preferably gutta-percha and root canal sealer/cement. The ideal termination for root canal preparation and obturation is just short of the radiographic apex of the toot. The rationale for this approach is well established and is designed to minimize periradicular inflammation and promote healing. Logically, over-instrumentation to the centre of a radiolucency, appears to violate the principles of non-surgical root canal treatment and the ideal management of the terminus. of .the root canal. However, the passage of small instruments past the end of the root canal would not substantially alter the morphology of the constriction. The procedure may injure some of the periradicular cells but the benefits of drainage and pressure release may outweigh trauma to the tissues. One successful approach to the clinical management of the large periradicular lesion has been calcium hydroxide used as an interim dressing. The rationale for the use of calcium hydroxde appears to be well-grounded after more than 50 years. The product has an antibacterial effect and germs coming in contact with the paste are easily destroyed by the high pH. Moreover,it has an active influnce on the local enviroment of resorption areas by making osteoclastic activity impossible and stimulating repair.It is well-known that hard tissue resorption,with its enzymatic activity, takes place in an acid pH. Calcium hyroxyde creates an alkalyne enviroment in which this reaction is reversed and hard tissue deposition can take place. When calcium hydroxide is used as an intracanal dressing or intermediate filling, its placement beyond the confines of the root canal and into the periradicular lesion has been advocated, as it has been speculated that the calcium hydroxide will have a direct affect on inflamed tissue and epithelial cystic linings. It has been postulated that the necrotizing ability of the calcium hydroxide may destroy any epithelium present, thereby allowing a connective tissue invagination into the lesion with ultimate healing. In contrast, other workers have suggested that the action of the calcium hydroxide beyond the apex may be fourfold: (i) antiinflammatory through its hygroscopic action, formation of calcium proteinate bridges, and inhibition of phospholipase; (ii) neutralization of acid products, such as acid hydrolases, which may affect clastic activity; (iii) activation of alkaline phosphatase; and (iv) antibacterial action. Although the exact biological rationale has been presented for the non-surgical endodontic management of periradicular pathosis of pulpal origin. Crucial to this management and ultimate success is the complete debridement of the root canal system, followed by three-dimensional obturation to seal both the apical foramen and coronal orifice. The potential mechanisms for cystic degeneration and tissue repair have been highlighted and the use of calcium hydroxide in this process has been discussed and suggested. Bibliografy
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